scholarly journals A general model to calculate the spin-lattice (T1) relaxation time of blood, accounting for haematocrit, oxygen saturation and magnetic field strength

2015 ◽  
Vol 36 (2) ◽  
pp. 370-374 ◽  
Author(s):  
Patrick W Hales ◽  
Fenella J Kirkham ◽  
Christopher A Clark

Many MRI techniques require prior knowledge of the T1-relaxation time of blood ( T1 bl). An assumed/fixed value is often used; however, T1 bl is sensitive to magnetic field ( B0), haematocrit ( Hct), and oxygen saturation ( Y). We aimed to combine data from previous in vitro measurements into a mathematical model, to estimate T1 bl as a function of B0, Hct, and Y. The model was shown to predict T1 bl from in vivo studies with a good accuracy (±87 ms). This model allows for improved estimation of T1 bl between 1.5–7.0 T while accounting for variations in Hct and Y, leading to improved accuracy of MRI-derived perfusion measurements.

1983 ◽  
Vol 14 (18) ◽  
Author(s):  
C. H. WOMACK ◽  
R. T. JUN. GAMPE ◽  
B. K. LEMKE ◽  
K. N. SAWHNEY ◽  
T. L. LEMKE ◽  
...  

1982 ◽  
Vol 19 (5) ◽  
pp. 1105-1107 ◽  
Author(s):  
Charles H. Womack ◽  
Robert T. Gampe ◽  
B. Kaye Lemke ◽  
Kailash N. Sawhney ◽  
Thomas L. Lemke ◽  
...  

1962 ◽  
Vol 17 (3) ◽  
pp. 552-558 ◽  
Author(s):  
Y. Enson ◽  
W. A. Briscoe ◽  
M. L. Polanyi ◽  
A. Cournand

An oximeter is described which employs two bundles of flexible glass fibers to conduct appropriately filtered light into, and that light diffusely reflected by the blood out of, the blood stream for the determination of oxygen saturation or dye concentration within blood flowing past the tip of either an arterial needle or a cardiac catheter which contains both bundles. The ratio of intensities of the reflected light at two wavelengths is linearly related to oxygen saturation (IRR805/ IRR660) and dye concentration (IRR900/IRR805). Data is reported in vivo and in vitro with respect to accuracy of the determinations (± 1.9%). The effect of patient-to-patient variation in hematocrit and other factors, and of pulsatile blood flow, is described. Application of the technique to physiologic study is illustrated, and theoretical aspects of reflection oximetry, as they apply to the instrument, are discussed. Submitted on November 17, 1961


2001 ◽  
Vol 5 (8) ◽  
pp. 645-651
Author(s):  
M. Peeva ◽  
M. Shopova ◽  
U. Michelsen ◽  
D. Wöhrle ◽  
G. Petrov ◽  
...  
Keyword(s):  

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S198-S198
Author(s):  
Joseph R Meno ◽  
Thien-son K Nguyen ◽  
Elise M Jensen ◽  
G Alexander West ◽  
Leonid Groysman ◽  
...  

1994 ◽  
Vol 72 (06) ◽  
pp. 942-946 ◽  
Author(s):  
Raffaele Landolfi ◽  
Erica De Candia ◽  
Bianca Rocca ◽  
Giovanni Ciabattoni ◽  
Armando Antinori ◽  
...  

SummarySeveral “in vitro” and “in vivo” studies indicate that heparin administration may affect platelet function. In this study we investigated the effects of prophylactic heparin on thromboxane (Tx)A2 biosynthesis “in vivo”, as assessed by the urinary excretion of major enzymatic metabolites 11-dehydro-TxB2 and 2,3-dinor-TxB2. Twenty-four patients who were candidates for cholecystectomy because of uncomplicated lithiasis were randomly assigned to receive placebo, unfractionated heparin, low molecular weight heparin or unfractionaed heparin plus 100 mg aspirin. Measurements of daily excretion of Tx metabolites were performed before and during the treatment. In the groups assigned to placebo and to low molecular weight heparin there was no statistically significant modification of Tx metabolite excretion while patients receiving unfractionated heparin had a significant increase of both metabolites (11-dehydro-TxB2: 3844 ± 1388 vs 2092 ±777, p <0.05; 2,3-dinor-TxB2: 2737 ± 808 vs 1535 ± 771 pg/mg creatinine, p <0.05). In patients randomized to receive low-dose aspirin plus unfractionated heparin the excretion of the two metabolites was largely suppressed thus suggesting that platelets are the primary source of enhanced thromboxane biosynthesis associated with heparin administration. These data indicate that unfractionated heparin causes platelet activation “in vivo” and suggest that the use of low molecular weight heparin may avoid this complication.


2020 ◽  
Vol 72 (5) ◽  
Author(s):  
Mario Fadin ◽  
Maria C. Nicoletti ◽  
Marzia Pellizzato ◽  
Manuela Accardi ◽  
Maria G. Baietti ◽  
...  
Keyword(s):  

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